A5001497525- Eosinophilic Esophagitis
- Immune Cell Function and Interaction
- IL-33, ST2, and ILC Pathways
- T-cell and B-cell Immunology
- Whipple's Disease and Interleukins
- Eosinophilic Disorders and Syndromes
- Esophageal and GI Pathology
- Mitochondrial Function and Pathology
- Cancer Immunotherapy and Biomarkers
- Gastroesophageal reflux and treatments
- Food Allergy and Anaphylaxis Research
- Microscopic Colitis
- Mast cells and histamine
- Contact Dermatitis and Allergies
- Metabolomics and Mass Spectrometry Studies
- Gut microbiota and health
- Parasitic infections in humans and animals
- Immunodeficiency and Autoimmune Disorders
- Immune Response and Inflammation
- Inflammatory Bowel Disease
Cornell University
2024
University of Michigan
2020-2024
Cincinnati Children's Hospital Medical Center
2018
University of Cincinnati
2018
Innate lymphoid cells (ILCs) can promote host defense, chronic inflammation, or tissue protection and are regulated by cytokines neuropeptides. However, their regulation diet microbiota-derived signals remains unclear. We show that an inulin fiber promotes Tph1-expressing inflammatory ILC2s (ILC2INFLAM) in the colon, which produce IL-5 but not tissue-protective amphiregulin (AREG), resulting accumulation of eosinophils. This exacerbates inflammation a murine model intestinal damage ILC2-...
Susceptibility to inflammatory bowel diseases (IBDs), Crohn's disease (CD), and ulcerative colitis (UC) is linked with loss of intestinal epithelial barrier integrity mitochondria dysfunction. Steroidogenic acute regulatory (StAR) protein-related lipid transfer (START) domain-containing protein 7 (STARD7) a phosphatidylcholine-specific (PC-specific) that transports PC from the ER mitochondria, facilitating membrane stabilization respiration function. The aim this study was define...
Group 3 innate lymphoid cells (ILC3s) are abundant in the developing or healthy intestine to critically support tissue homeostasis response microbial colonization. However, intestinal ILC3s reduced during chronic infections, colorectal cancer, inflammatory bowel disease (IBD), and mechanisms driving these alterations remain poorly understood. Here we employed RNA sequencing of from IBD patients observed a significant upregulation RIPK3, central regulator necroptosis, inflammation. This was...
Background & AimsCD4+ T cells are regulated by activating and inhibitory cues, dysregulation of these proper regulatory inputs predisposes to aberrant inflammation exacerbation disease. We investigated the role receptor paired immunoglobulin-like B (PIR-B) in regulation CD4+ T-cell inflammatory response colitic phenotype.MethodsWe used Il10-/- spontaneous CD4+CD45RBhi transfer models colitis with PIR-B-deficient (Pirb-/-) mice. Flow cytometry, Western blot, RNA sequencing analysis was...
Abstract Rationale CD4+T-cell differentiation into effector or memory populations is intrinsically regulated by the delicate balance between activating and inhibitory signals. Previously we identified a role of receptor, Paired Immunoglobulin-like Receptor (PIR) B in negative regulation innate immune responses colitis. The aim this study to define involvement PIRB CD4+ Th17 development Th17-dependent Results We demonstrate an intrinsic deficiency PirB−/− vitro polarization cell survival....